Hypertriglyceridemia: A Review of Clinical Relevance and Treatment Options: Focus on Cerivastatin

Hans-Willi M. Breuer, Abteilung für Innere Medizin, St. Carolus-Krankenhaus Görlitz, Carolusstr. 212, 02827 Görlitz, Germany 

Curr Med Res Opin. 2001;17(1):60-73. 

In This Article

Mode of Pathogenesis

It is thought that in type IIb dyslipidemia, smaller VLDL-C and chylomicron remnants are formed from TG-rich VLDL and chylomicrons and it is these remnants that are considered to be highly atherogenic[6]. The exact role of TG in CHD pathogenesis is not clear, but is thought to involve several direct and indirect mechanisms including effects on the metabolism of other lipoproteins,transport proteins and enzymes and the coagulation system (Figure 3)[1,27,28,45,59,60,61,62].

The role of TG in CHD pathogenesis

The role of TG in atherogenesis may involve some or all of the following:

  • Synthesis of prothrombotic factors, such as fibrinogen and plasminogen activator inhibitors,leading to a variety of coagulation defects(alternatively, increased TG levels and coagulation defects may both be the result of a more generalised metabolic disorder[41]).

  • Modifications in the metabolism of HDL-C and LDLs to produce high LDL-C and low HDL-C levels and increased levels of atherogenic TGRLPs such as small, dense LDL-C[21]. Conversely,normal TG levels are associated with large buoyant LDL-C particles, which are an important predictor in coronary disease regression[45,49,55].

  • An increase in cell adhesion molecules and decreased artery flow-mediated vasodilation,both of which are implicated in endothelial dysfunction, is itself thought to be an early sign of atherosclerosis[60].

  • Increased VLDL-apolipoprotein B (apoB)production and cholesterol synthesis[62].

  • Increase in TG- and cholesterol-rich lipoprotein remnants thought to be utilised by intimal macrophages to form foam cells (seen in early stage atherosclerotic plaque formation)[45].

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